If so, repetitive mechanical stimulation of airways irritant receptors may have led to vagally mediated reflex bronchoconstriction. Alternatively, there is experimental evidence that a quick stretch will increase tension in isolated sensitized airways smooth muscle. If this is true in vivo, repetitive stretching of airway smooth muscle may have contributed to post-M W reductions in SGaw in our asthmatic subjects. Source
There are other possible explanations for reduced airway caliber after a series of deep breaths. Cooling of the airways as well as loss of humidity during MW maneuvers might increase bronchomotor tone in asthmatic subjects. On the other hand, relatively little respiratory heat and water transfer would be expected during 12 s of hyperventilation. Changes in end-tidal carbon dioxide tension (PETC02) consequent to hyperventilation also might cause bronchoconstric-tion during MW maneuvers. Previous studies have demonstrated that resistance to airflow increased as PETC02 decreased, although hyperventilation challenges and exercise still precipitate bronchocon-striction when COz is added to the inspired air.
On the other hand, the effects of hypocarbia are small until PETC02 approximates 25 mm Hg or less. In our asthmatic subjects, MW was measured using a closed-circuit system; this would have minimized changes in PETC02 (and in respiratory heat and water transfer). Fatigue and/or decreased endurance of respiratory muscles may also have caused or contributed to low MW values in the asthmatic subjects. In this regard, higher lung volumes in the asthmatic subjects may have caused a mechanical disadvantage of the inspiratory muscles. On the other hand, this was probably not a major determinant of differences in MW since the differences between Vtg in the normals and asthmatic subjects were (although statistically significant) quantitatively small.